34 AIR POLLUTANT EFFECTS
the occurrence of lasting atmospheric inversions resulted in
thousands of excess deaths.CARBON MONOXIDECarbon monoxide has afflicted the human race since the
discovery of fire. Nature contributes very significant quanti-
ties, but it does so in such a highly dispersed fashion that
human exposures from this source are insignificant. Nature
has provided sinks for this insoluble, relatively unreactive
gas; otherwise background concentrations would rise much
more rapidly as human contributions added their burden. The
oceans, which at one time were believed to be a major sink,
are now considered to be a source, because certain marine
organisms release enough carbon monoxide to supersatu-
rate the surface layer. The important removal mechanism
is believed to be the action of microorganisms that live in
soils and plants and the reaction of carbon monoxide with
hydroxyl radicals in the atmosphere.
The rapid growth in the use of internal combustion
engines has created an outdoor problem as indoor problems
were decreased by improvements in space-heating equip-
ment. The problem is concentrated in urban areas where traf-
fic congestion is combined with canyonlike streets. Emissions
of carbon monoxide in the United States decreased from 197
million tons in 1970 to 94 million tons in 2003.
With the exception of exposures resulting from the break-
down or misuse of indoor heating equipment that produces
fatalities or serious injuries, carbon-monoxide exposures
of significance occur in the vicinity of congested traffic.
People whose occupation requires them to be near such traf-
fic receive the highest exposures, as do those who jog or
bicycle in these areas. Malfunctions in the exhaust system of
vehicles also can result in high exposures to their occupants.
Exposure to carbon monoxide results in the buildup of car-
boxyhemoglobin in the blood, which will interfere with the
transport of oxygen to cells in the body.
Carbon-monoxide molecules attach themselves to the
hemoglobin molecules in the blood with much greater
tenacity than do oxygen molecules. The Haldane equation
attempts to approximate this competition.(HbCO)
(HbO )210PCO2 PO 2(HbCO) and (HbO 2 ) are the concentrations of carboxyhemo-
globin and oxyhemoglobin, and PCO and PO 2 are the partial
pressures of carbon monoxide and oxygen. Inspiration of air
containing high concentrations of carbon monoxide results
in its preferential absorption in the blood, thereby interfering
with oxygen delivery to the cells in the body. Exposure to
carbon monoxide causes a gradual increase in the percentage
of carboxyhemoglobin in the blood until an equilibrium value
dependent upon the ambient air concentration is reached. The
rate of intake is dependent upon the breathing rate; therefore,
equilibrium is reached more quickly the greater the exertion.Up to 50 ppm, the equilibrium values of carboxyhemoglobin
corresponding to different concentrations of inspired carbon
monoxide can be estimated from the equation%HbCO 0.4PPM CO
7 The 0.4 constant is in the equation to account for the endog-
enous carbon monoxide, that is, the carboxyhemoglobin that
results from the body’s own production of carbon monoxide.
Graphic representations of the conversion of hemoglo-
bin to carboxyhemoglobin in the presence of different con-
centrations of ambient carbon monoxide and the effect of
various levels of activity on the rate of uptake are presented
in Figure 2 and Figure 3.
The level of HbCO in the blood (Table 2) is the impor-
tant measurement in the evaluation of carbon-monoxide pol-
lution. High levels of HbCO are associated with cigarette
smokers, firemen, garage workers, foundry workers, and
individuals who spend extended periods of time in heavy
congested traffic or in vehicles with faulty exhaust systems.
Ambient carbon-monoxide measurements at a monitoring
site can be very misleading as an index of exposure, because
study populations are usually mobile and carbon-monoxide
concentrations can vary significantly, both horizontally and
vertically, throughout an urban area.
Exposures to the high concentrations of carbon monox-
ide sometimes encountered in community atmospheres, even
those well above the national standards, are not believed to
be sufficient to initiate cardiopulmonary disease; however,
individuals whose pulmonary functions are already signifi-
cantly impaired because of anemia or damage to the heart,
vascular system, or lungs can suffer adverse health effects
from such exposures.
In order to maintain normal function, the tissues of the
body must receive oxygen at a rate that depends upon their
nature and functions. Those with a high rate of oxygen demand
are more susceptible to the oxygen-depriving action of carbon
monoxide. For example, studies of the brain and liver show
a decrease in oxygen pressure at those sites even at levels
as low as 2% carboxyhemoglobin. Cardiopulmonary-system
abnormalities, such as shunts that have developed that allow
venous blood to mix directly with arterial blood, cause the
individuals affected to be explicitly sensitive to carbon mon-
oxide. Angina-pectoris patients who experienced exposures
that raised their carboxyhemoglobin level to 2.5%—that is,
approximately to the level produced by an 8-hour exposure at
the concentration set as the air-quality standard—suffered the
onset of chest pain from exercise significantly sooner than did
other angina patients not similarly exposed. The reduction in
risk of heart attack that is observed soon after the cessation of
the cigarette-smoking habit indicates that carbon monoxide
may be an important factor in precipitating heart attacks. The
inhalation of carbon monoxide during pregnancy is a special
concern because a higher concentration of carboxyhemoglo-
bin is generated in the fetus than in the mother, and the elimi-
nation of carbon monoxide after exposure is slower in theC001_003_r03.indd 34 11/22/2005 11:06:05 AM